ATM controls DNA repair and mitochondria transfer between neighboring cells

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Sha Jin - , OncoRay - National Centre for Radiation Research in Oncology (Author)
  • Nils Cordes - , OncoRay - National Center for Radiation Research in Oncology, Department of Radiotherapy and Radiooncology, University Vascular Centre, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), OncoRay - National Centre for Radiation Research in Oncology , Heidelberg University , German Cancer Research Center (DKFZ), German Cancer Consortium (DKTK) Partner Site Dresden, German Center for Neurodegenerative Diseases (DZNE) - Partner Site Dresden (Author)

Abstract

Intercellular communication is essential for multicellular tissue vitality and homeostasis. We show that healthy cells message protective signals through direct cell-cell connections to adjacent DNA-damaged cells in a microtubule-dependent manner. In DNA-damaged cells, mitochondria restoration is facilitated by fusion with undamaged mitochondria from healthy cells and their DNA damage repair is optimized in presence of healthy cells. Both, mitochondria transfer and intercellular signaling for an enhanced DNA damage response are critically regulated by the activity of the DNA repair protein ataxia telangiectasia mutated (ATM). These healthy-to-damaged prosurvival processes sustain normal tissue integrity and may be exploitable for overcoming resistance to therapy in diseases such as cancer.

Details

Original languageEnglish
Pages (from-to)144
JournalCell Communication and Signaling
Volume17
Issue number1
Publication statusPublished - 8 Nov 2019
Peer-reviewedYes

External IDs

PubMedCentral PMC6842230
Scopus 85074702360
ORCID /0000-0001-5684-629X/work/146646170

Keywords

Sustainable Development Goals

Keywords

  • Ataxia Telangiectasia Mutated Proteins/metabolism, Cell Cycle, Cell Line, Tumor, Coculture Techniques, DNA Damage, DNA Repair, Humans, Microtubules/metabolism, Mitochondria/metabolism, Signal Transduction